7
Abdominal compartment syndrome Manu Malbrain Address: ZNA Stuivenberg, Lange Beeldekensstraat 267, B-2060 Antwerpen 6, Belgium Email: [email protected] F1000 Medicine Reports 2009, 1:86 (doi:10.3410/M1-86) The electronic version of this article is the complete one and can be found at: http://F1000.com/Reports/Medicine/content/1/86 Abstract The abdominal compartment syndrome (ACS) was first described in surgical patients with abdominal aortic aneurysm repair, trauma, bleeding, or infection, but in recent years it has also been described in patients with other pathologies such as burn injury and sepsis and in medical patients. This F1000 Medicine Report is intended to provide critical care physicians a clear insight into the current state of knowledge regarding intra-abdominal hypertension (IAH) and ACS, and will focus primarily on the recent literature as well as on the definitions and recommendations published by the World Society of the Abdominal Compartment Syndrome. The definitions regarding increased intra- abdominal pressure (IAP) will be listed, followed by a brief but comprehensive overview of the different mechanisms of organ dysfunction associated with IAH. The gold standard measurement technique for IAP as well as recommendations for organ function support in patients with IAH and options for medical and surgical treatment of IAH and ACS will be discussed. Introduction and context A compartment syndrome exists when the increased pressure in a closed anatomic space threatens the viability of surrounding tissue. When this occurs in the abdomen, the impact on end-organ function within and outside the cavity can be devastating. The abdominal compartment syndrome (ACS) is not a disease; as such, it can have many causes and can develop within many disease processes. It is only recently that ACS has received heightened attention [1]. The prevention of intra-abdominal hyper- tension (IAH) and ACS is of tremendous importance in the care of critically ill, surgical, and trauma patients. Serial intra-abdominal pressure (IAP) measurements are essential to the diagnosis, management, and fluid resuscitation of these patients. Clinical examination is not an accurate method to estimate IAP [2]. Intravesicular pressure is a good estimate for IAP, is easily measured, and should be monitored in all patients believed to be at risk for significant elevations in IAP [3-6]. The management of IAH is based on four principles [3-6] (Figure 1): (a) serial monitoring of IAP; (b) optimization of systemic perfusion and organ function in the patient with elevated IAP; (c) institution of specific medical procedures to reduce IAP and the end-organ conse- quences of IAH/ACS; (d) prompt surgical decompression for refractory IAH. Recent advances Recently, the World Society of the Abdominal Compart- ment Syndrome (WSACS) [7] published the consensus definitions and recommendations regarding the diag- nosis and management of IAH and ACS [4,5]. Consensus definitions Intra-abdominal pressure: IAP is the steady-state pressure concealed within the abdominal cavity. It is directly affected by the volume of the solid organs or hollow viscera (which may be either empty or filled with air, liquid, or fecal matter), the presence of ascites, blood or other space-occupying lesions (such as tumors or a gravid uterus), and the presence of conditions that limit expansion of the abdominal wall (such as burn eschars or third-space edema). The respiratory variation seen in the IAP tracing is an indirect measurement of abdominal wall compliance [8]. Page 1 of 7 (page number not for citation purposes) Published: 16 November 2009 © 2009 Medicine Reports Ltd

Abdominal compartment syndromef1000researchdata.s3.amazonaws.com/f1000reports/files/9008/1/86… · A compartment syndrome exists when the increased pressure in a closed anatomic

  • Upload
    others

  • View
    0

  • Download
    0

Embed Size (px)

Citation preview

Page 1: Abdominal compartment syndromef1000researchdata.s3.amazonaws.com/f1000reports/files/9008/1/86… · A compartment syndrome exists when the increased pressure in a closed anatomic

Abdominal compartment syndromeManu Malbrain

Address: ZNA Stuivenberg, Lange Beeldekensstraat 267, B-2060 Antwerpen 6, Belgium

Email: [email protected]

F1000 Medicine Reports 2009, 1:86 (doi:10.3410/M1-86)

The electronic version of this article is the complete one and can be found at: http://F1000.com/Reports/Medicine/content/1/86

Abstract

The abdominal compartment syndrome (ACS) was first described in surgical patients with abdominalaortic aneurysm repair, trauma, bleeding, or infection, but in recent years it has also been describedin patients with other pathologies such as burn injury and sepsis and in medical patients. ThisF1000 Medicine Report is intended to provide critical care physicians a clear insight into the currentstate of knowledge regarding intra-abdominal hypertension (IAH) and ACS, and will focus primarilyon the recent literature as well as on the definitions and recommendations published by the WorldSociety of the Abdominal Compartment Syndrome. The definitions regarding increased intra-abdominal pressure (IAP) will be listed, followed by a brief but comprehensive overview of thedifferent mechanisms of organ dysfunction associated with IAH. The gold standard measurementtechnique for IAP as well as recommendations for organ function support in patients with IAH andoptions for medical and surgical treatment of IAH and ACS will be discussed.

Introduction and contextA compartment syndrome exists when the increasedpressure in a closed anatomic space threatens the viabilityof surrounding tissue. When this occurs in the abdomen,the impact on end-organ function within and outside thecavity can be devastating. The abdominal compartmentsyndrome (ACS) is not a disease; as such, it can havemanycauses and can develop within many disease processes. Itis only recently that ACS has received heightenedattention [1]. The prevention of intra-abdominal hyper-tension (IAH) and ACS is of tremendous importance inthe care of critically ill, surgical, and trauma patients.Serial intra-abdominal pressure (IAP) measurements areessential to the diagnosis, management, and fluidresuscitation of these patients. Clinical examination isnot an accurate method to estimate IAP [2]. Intravesicularpressure is a good estimate for IAP, is easily measured, andshould be monitored in all patients believed to be at riskfor significant elevations in IAP [3-6].

The management of IAH is based on four principles [3-6](Figure 1): (a) serial monitoring of IAP; (b) optimizationof systemic perfusion and organ function in the patient

with elevated IAP; (c) institution of specific medicalprocedures to reduce IAP and the end-organ conse-quences of IAH/ACS; (d) prompt surgical decompressionfor refractory IAH.

Recent advancesRecently, the World Society of the Abdominal Compart-ment Syndrome (WSACS) [7] published the consensusdefinitions and recommendations regarding the diag-nosis and management of IAH and ACS [4,5].

Consensus definitionsIntra-abdominal pressure: IAP is the steady-state pressureconcealed within the abdominal cavity. It is directlyaffected by the volume of the solid organs or hollowviscera (which may be either empty or filled with air,liquid, or fecal matter), the presence of ascites, blood orother space-occupying lesions (such as tumors or agravid uterus), and the presence of conditions that limitexpansion of the abdominal wall (such as burn escharsor third-space edema). The respiratory variation seen inthe IAP tracing is an indirect measurement of abdominalwall compliance [8].

Page 1 of 7(page number not for citation purposes)

Published: 16 November 2009© 2009 Medicine Reports Ltd

Page 2: Abdominal compartment syndromef1000researchdata.s3.amazonaws.com/f1000reports/files/9008/1/86… · A compartment syndrome exists when the increased pressure in a closed anatomic

Figure 1. Intra-abdominal hypertension/abdominal compartment syndrome management algorithm of the World Society of theAbdominal Compartment Syndrome

ACS, abdominal compartment syndrome; APP, abdominal perfusion pressure; CVP, central venous pressure; CVPtm, transmural central venous pressure; IAH,intra-abdominal hypertension; IAP, intra-abdominal pressure; MAP, mean arterial pressure; PAOP, pulmonary artery occlusion pressure; PAOPtm, transmuralpulmonary artery occlusion pressure; Pplat, plateau pressure; Pplattm, transmural plateau pressure. Adapted from [4,5]. Copyright 2006, 2007, SpringerBerlin/Heidelberg.

Page 2 of 7(page number not for citation purposes)

F1000 Medicine Reports 2009, 1:86 http://F1000.com/Reports/Medicine/content/1/86

Page 3: Abdominal compartment syndromef1000researchdata.s3.amazonaws.com/f1000reports/files/9008/1/86… · A compartment syndrome exists when the increased pressure in a closed anatomic

Perfusion: Analogous to the widely accepted andclinically used concept of cerebral perfusion pressure[calculated as mean arterial pressure (MAP) minusintracranial pressure (ICP)], abdominal perfusion pres-sure (calculated as MAP minus IAP) has been proposedas a more accurate predictor of visceral perfusion and apotential endpoint for resuscitation [9]. Althoughpatients with IAH need to be well resuscitated, there isa lot of debate regarding futile crystalloid over-resuscita-tion and the development of secondary IAH [10].

Measurement: The reference standard for intermittentIAP measurement is via the bladder with a maximalinstillation volume of 20-25 mL of sterile saline. The IAPshould be expressed in millimeters of mercury (mm Hg)and measured at end-expiration in the complete supineposition after the clinician ensures that abdominalmuscle contractions are absent and that the transduceris zeroed at the level of the midaxillary line. Recentstudies have examined the effect of different zeroreference and head-of-bed positions on IAP [11,12].

Normal values: Normal IAP is approximately 5-7 mmHgin critically ill adults. IAP may be increased to 12-15 mmHg in postoperative patients. Chronic IAP elevations canbe seen in liver cirrhosis with ascites, large ovariantumors, pregnancy, chronic ambulatory peritoneal dia-lysis (CAPD), or obesity.

Intra-abdominal hypertension: IAH is defined as asustained or repeated pathologic elevation of IAP ofgreater than 12 mm Hg [4]. IAH is graded as follows:grade I, IAH of 12-15 mmHg; grade II, IAH of 16-20 mmHg; grade III, IAH of 21-25 mm Hg; and grade IV, IAH ofgreater than 25 mm Hg. It should be noted that the IAPranges associated with these grades have been reviseddownward in recent years as the detrimental impact ofelevated IAP on end-organ function has been recognized.Table 1 lists some risk factors for the development ofIAH.

Abdominal compartment syndrome: ACS is defined as asustained IAP of at least 20 mm Hg that is associatedwith new organ dysfunction/failure.

The WSACS suggests the following classification for IAH:Primary IAH is a condition associated with injury ordisease in the abdomino-pelvic region which frequentlyrequires early surgical or radiological intervention.Secondary IAH is a condition that does not originatefrom the abdomino-pelvic region. Recurrent IAH is acondition in which IAH/ACS redevelops followingprevious surgical or medical treatment of primary orsecondary IAH/ACS.

Further classification can be done in relation to the timecourse of the events: chronic IAH (occurring over thecourse of months to years) as seen with morbid obesity,intra-abdominal tumor (large ovarian cyst, fibroma, andso on), chronic ascites (liver cirrhosis or CAPD), orpregnancy; in those cases, the abdominal wall adaptsprogressively during months or years to the increase inIAP and allows time for the body to adapt. Acute IAH isdue mainly to trauma or intra-abdominal hemorrhage ofany cause and leads to ACS within hours. Subacute IAHis seen with most medical cases in the intensive care unitthat lead to IAH within days and results from a

Table 1. Risk factors for the development of intra-abdominalhypertension and abdominal compartment syndrome

A. Related to diminished abdominal wall compliance- Mechanical ventilation, especially fighting with the ventilator and the

use of accessory muscles- Use of positive end-expiratory pressure (PEEP) or the presence of

auto-PEEP- Basal pleuropneumonia- High body mass index- Pneumoperitoneum- Abdominal (vascular) surgery, especially with tight abdominal closures- Pneumatic anti-shock garments- Prone and other body positioning- Abdominal wall bleeding or rectus sheath hematomas- Correction of large hernias, gastroschisis, or omphalocoele- Burns with abdominal eschars

B. Related to increased intra-abdominal contents- Gastroparesis- Gastric distention- Ileus- Volvulus- Colonic pseudo-obstruction- Abdominal tumor- Retroperitoneal/abdominal wall hematoma- Enteral feeding- Intra-abdominal or retroperitoneal tumor- Damage control laparotomy

C. Related to abdominal collections of fluid, air, or blood- Liver dysfunction with ascites- Abdominal infection (pancreatitis, peritonitis, abscess, and so on)- Hemoperitoneum- Pneumoperitoneum- Laparoscopy with excessive inflation pressures- Major trauma- Peritoneal dialysis

D. Related to capillary leak and fluid resuscitation- Acidosisa (pH <7.2)- Hypothermiaa (core temperature <33°C)- Coagulopathya (platelet count <50,000/mm3 OR an activated partial

thromboplastin time more than two times normal OR a prothrombin time<50% OR an international standardised ratio >1.5)- Polytransfusion/trauma (>10 units of packed red cells per 24 hours)- Sepsis (as defined by the American-European Consensus Conference

definitions)- Severe sepsis or bacteremia- Septic shock- Massive fluid resuscitation (>5 L of colloid or >10 L of crystalloid per

24 hours with capillary leak and positive fluid balance)- Major burns

a The combination of acidosis, hypothermia, and coagulopathy has beenforwarded in the literature as the deadly triad leading to abdominalcompartment syndrome.

Page 3 of 7(page number not for citation purposes)

F1000 Medicine Reports 2009, 1:86 http://F1000.com/Reports/Medicine/content/1/86

Page 4: Abdominal compartment syndromef1000researchdata.s3.amazonaws.com/f1000reports/files/9008/1/86… · A compartment syndrome exists when the increased pressure in a closed anatomic

combination of etiologic factors and predisposingconditions. Hyperacute IAH lasts for only a very shortperiod (seconds or minutes) as with laughing, straining,coughing, sneezing, defecating, or performing physicalactivity and has no clinical implications.

Implications for clinical practiceOrgan supportFigure 2 lists the effects of IAH/ACS on end-organfunction [13]. In the paragraphs below, some key pointsto remember are listed [14].

Figure 2. Impact of increased intra-abdominal pressure on end-organ function

1Cardiovascular effects are exacerbated in case of hypovolemia, hemorrhage, ischemia, and ventilation with high positive end-expiratory pressure (PEEP).CAPD, continuous ambulatory peritoneal dialysis; FiO2, fraction of inspired oxygen; IL, interleukin; PaO2, arterial partial pressure of oxygen; TNF-a, tumornecrosis factor-alpha.

Page 4 of 7(page number not for citation purposes)

F1000 Medicine Reports 2009, 1:86 http://F1000.com/Reports/Medicine/content/1/86

Page 5: Abdominal compartment syndromef1000researchdata.s3.amazonaws.com/f1000reports/files/9008/1/86… · A compartment syndrome exists when the increased pressure in a closed anatomic

For the brain [15-17]: IAH/ACS will increase ICP anddecrease cerebral perfusion pressure. Because of theinteractions between IAP, intrathoracic pressure (ITP),and ICP, accurate monitoring of IAP in head traumavictims with associated abdominal lesions is worthwhile.The presence of increased IAP can be an additional‘extracranial’ cause of intracranial hypertension (ICH) inpatients with abdominal trauma without overt cranio-cerebral lesions. Laparoscopy should be avoided inpatients with ICH. Obesity causes idiopathic ICH, andweight loss after bariatric surgery is associated withimprovements in ICP and symptoms. The direct effectsof IAH on neurologic function can be ablated bysternotomy, pericardiotomy, or bilateral pleurotomy[18]. Recently, IAH has been related to ventriculoper-itoneal shunt dysfunction [19].

For the heart [20-23]: The clinician must be aware ofthe polycompartment syndrome and the interactionsbetween ITP, IAP, positive end-expiratory pressure(PEEP), and intracardiac filling pressures. Use transmuralfilling pressures as a preload estimate, calculated as theend-expiration value minus the ITP: transmural centralvenous pressure (CVPtm) = end-expiration central venouspressure (CVPee) – ITP, or transmural pulmonary arteryocclusion pressure (PAOPtm) = end-expiration pulmon-ary artery occlusion pressure (PAOPee) – ITP. The averageabdomino-thoracic transmission is around 50%. A quickestimate of transmural filling pressures can also beobtained by subtracting half of the IAP from the end-expiratory filling pressure, or CVPtm = CVPee –½ IAP andPAOPtm = PAOPee – ½ IAP. Maybe the Surviving SepsisCampaign guidelines for initial and ongoing resuscita-tion should be guided toward a CVPtm of 8-12 mm Hgand a transmural MAP of 65 mm Hg to avoidunnecessary over- and under-resuscitation. Use volu-metric estimates of preload status to take into accountthe changing ventricular compliance and elevated ITP:right ventricular end-diastolic volume index or globalend-diastolic volume index. Functional hemodynamicparameters such as stroke volume variation or pulsepressure variation, but not systolic pressure variation,should be used to assess volume responsiveness.

For the lungs [24-26]: As a rule of thumb, the best PEEPmay be set to counteract IAP whilst at the same timeavoiding overinflation of already well-aerated lungregions. The best PEEP (cm H2O) = IAP (mm Hg) to amaximum value of 20. This holds especially true in thesetting of secondary acute respiratory distress syndromerelated to abdominal problems (with IAH). In case ofACS with an IAP of greater than 20 mm Hg, all medicaland surgical options to lower IAP and restore end-organ

perfusion should be performed. Plateau pressures(Pplat) should be limited to transmural plateau pres-sures (Pplattm) of below 35 cm H2O: Pplattm = Pplat –½IAP. IAH will lead to pulmonary hypertension andincreases lung edema in case of capillary leak and fluidoverload. Therefore, monitoring extravascular lung waterindex may be worthwhile.

For the liver [27,28]: Monitor noninvasive hepatos-planchnic perfusion during IAH. Indocyanine greenplasma disappearance rate decreases during IAH [29].

For the kidneys [30-32]: Elevated IAP significantlydecreases renal artery blood flow and compresses therenal vein, leading to renal dysfunction and failure [33].Oliguria develops at an IAP of 15 mm Hg and anuria at30 mm Hg in the presence of normovolemia and atlower levels of IAP in the patient with hypovolemia orsepsis. Renal perfusion pressure (RPP) and renal filtra-tion gradient have been proposed as key factors in thedevelopment of IAP-induced renal failure (RPP = MAP –

IAP).

Changes in IAP have a greater impact upon renalfunction and urine production than do changes in

Table 2. Medical treatment options for abdominal compartmentsyndrome

1. Improvement of abdominal wall compliance- Sedation and pain relief (not fentanyl)- Neuromuscular blockade- Body positioning (avoid upright, use anti-Trendelenburg)- Negative fluid balance- Skin pressure decreasing interfaces- Weight loss- Percutaneous/endoscopic abdominal wall component separation

2. Evacuation of intraluminal contents- Gastric tube and suctioning- Gastroprokinetics (erythromycin, cisapride, metoclopramide)- Rectal tube and enemas- Colonoprokinetics (neostygmine, prostygmine bolus, or infusion)- Endoscopic decompression of large bowel- Colostomy or ileostomy

3. Evacuation of peri-intestinal and abdominal fluids- Paracenthesis or ascites evacuation- Computed tomography (CT)- or ultrasound-guided aspiration of

abscess- CT- or ultrasound-guided aspiration of hematoma- Percutaneous drainage of (blood/fluid) collections

4. Correction of capillary leak and positive fluid balance- Albumin 20% in combination with diuretics (furosemide)- Correction of capillary leak (antibiotics, source control, and so on)- Colloids instead of cristalloids- Dobutamine (not dopamine)- Dialysis or continuous venovenous hemofiltration with ultrafiltration- Ascorbinic acid in burn patients

5. Specific therapeutic interventions- Continuous negative abdominal pressure- Negative external abdominal pressure- Targeted perfusion pressure

� Target abdominal perfusion pressure >60 mm Hg

Page 5 of 7(page number not for citation purposes)

F1000 Medicine Reports 2009, 1:86 http://F1000.com/Reports/Medicine/content/1/86

Page 6: Abdominal compartment syndromef1000researchdata.s3.amazonaws.com/f1000reports/files/9008/1/86… · A compartment syndrome exists when the increased pressure in a closed anatomic

MAP. It should not be surprising, therefore, thatdecreased renal function, as evidenced by the develop-ment of oliguria, is one of the first visible signs of IAH.Therefore, it behooves us as clinicians to be cognizant ofthe elevated IAP, and its effect on renal function is oftenthe first sign of impending ACS. Recently, Dalfino andcolleagues [32] became the first to report a relationbetween RIFLE (Risk, Injury, Failure, Loss, and End-stagekidney disease) criteria for acute kidney injury and IAH.

Nonsurgical treatmentBefore surgical decompression is considered, less inva-sive medical treatment options should be optimized. Therelation between abdominal contents and IAP is notlinear but exponential, and this curve is shifted to the leftand upwards when abdominal wall compliance isdecreased. Therefore, IAH can be treated by improvingabdominal wall compliance and decreasing intra-abdominal volume or both. Different medical treatmentoptions have been suggested to decrease IAP; however, itmust be noted that, as of today, the evidence regardingthese recommendations is scarce and mostly based oncase reports and small cohort studies, whereas someevidence is based on speculation and non-evidence-based methods used in ileus and bowel obstruction.

Medical treatment is based on five different mechanisms:(a) improvement of abdominal wall compliance; (b)evacuation of intraluminal contents; (c) evacuation ofabdominal fluid collections; (d) correction of capillaryleak and positive fluid balance; and (e) specifictreatments (see Table 2 for more details).

Surgical treatmentDecompressive laparotomy is the definitive treatment forACS [34]. The technique can be invasive (midlinelaparotomy) or minimally invasive (endoscopic techni-ques based on subcutaneous anterior abdominal fas-ciotomy). This intervention results in a laparostomy oropen abdomen so that a temporary abdominal closureis needed (moist gauze, towel clip closure, Bogotabag, Wittman patch or zipper, home-made system, orvacuum-assisted closure). Figure 3 shows a surgicaltreatment algorithm.

AbbreviationsACS, abdominal compartment syndrome; CAPD,chronic ambulatory peritoneal dialysis; CVPee, end-expiration central venous pressure; CVPtm, transmuralcentral venous pressure; IAH, intra-abdominal hyperten-sion; IAP, intra-abdominal pressure; ICH, intracranialhypertension; ICP, intracranial pressure; ITP, intrathor-acic pressure; MAP, mean arterial pressure; PAOPee, end-expiration pulmonary artery occlusion pressure;PAOPtm, transmural pulmonary artery occlusion pres-sure; PEEP, positive end-expiratory pressure; Pplat,plateau pressures; Pplattm, transmural plateau pressure;RIFLE, Risk, Injury, Failure, Loss, and End-stage kidneydisease; RPP, renal perfusion pressure; WSACS, WorldSociety of the Abdominal Compartment Syndrome.

Competing interestsMM is a past president of the World Society of theAbdominal Compartment Syndrome, is a member of themedical advisory boards of Holtech Medical (Charlot-tenlund, Denmark), Spiegelberg (Hamburg, Germany),and Pulsion Medical Systems (Munich, Germany), hasreceived royalties from Holtech Medical and Spiegelberg,and holds a patent with Pulsion Medical Systems.

References1. Kimball EJ, Rollins MD, Mone MC, Hansen HJ, Baraghoshi GK,

Johnston C, Day ES, Jackson PR, Payne M, Barton RG: Survey ofintensive care physicians on the recognition and manage-ment of intra-abdominal hypertension and abdominal com-partment syndrome. Crit Care Med 2006, 34:2340-8.

2. Malbrain ML: Different techniques to measure intra-abdominalpressure (IAP): time for a critical re-appraisal. Intensive CareMed 2004, 30:357-71.

3. Malbrain ML, De laet I, Cheatham M: Consensus conferencedefinitions and recommendations on intra-abdominal hyper-tension (IAH) and the abdominal compartment syndrome

Figure 3. Surgical treatment algorithm for the patient withabdominal compartment syndrome (ACS)

ICU, intensive care unit; TAC, temporary abdominal closure; VAFC,vacuum-assisted fascial closure.

Page 6 of 7(page number not for citation purposes)

F1000 Medicine Reports 2009, 1:86 http://F1000.com/Reports/Medicine/content/1/86

Page 7: Abdominal compartment syndromef1000researchdata.s3.amazonaws.com/f1000reports/files/9008/1/86… · A compartment syndrome exists when the increased pressure in a closed anatomic

(ACS)–the long road to the final publications, how did we getthere? Acta Clin Belg Suppl 2007, 62:44-59.

4. Malbrain ML, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, DeWaele J, Balogh Z, Leppäniemi A, Olvera C, Ivatury R, D’Amours S,Wendon J, Hillman K, Johansson K, Kolkman K, Wilmer A: Resultsfrom the International Conference of Experts on Intra-abdominal Hypertension and Abdominal CompartmentSyndrome. I. Definitions. Intensive Care Med 2006, 32:1722-32.

5. Cheatham ML, Malbrain ML, Kirkpatrick A, Sugrue M, Parr M, DeWaele J, Balogh Z, Leppäniemi A, Olvera C, Ivatury R, D’Amours S,Wendon J, Hillman K, Wilmer A: Results from the InternationalConference of Experts on Intra-abdominal Hypertension andAbdominal Compartment Syndrome. II. Recommendations.Intensive Care Med 2007, 33:951-62.

6. De Waele JJ, De laet I, Malbrain ML: Rational intraabdominalpressure monitoring: how to do it? Acta Clin Belg Suppl 2007,62:16-25.

7. World Society of the Abdominal Compartment Syndromehomepage. [http://www.wsacs.org].

8. Sturini E, Saporito A, Sugrue M, Parr MJ, Bishop G, Braschi A:Respiratory variation of intra-abdominal pressure: indirectindicator of abdominal compliance? Intensive Care Med 2008,34:1632-7.

9. Cheatham ML, White MW, Sagraves SG, Johnson JL, Block EF:Abdominal perfusion pressure: a superior parameter in theassessment of intra-abdominal hypertension. J Trauma 2000,49:621-6; discussion 626-7.

10. Cheatham ML: Intraabdominal pressure monitoring duringfluid resuscitation. Curr Opin Crit Care 2008, 14:327-33.

11. De Waele JJ, De Laet I, De Keulenaer B, Widder S, Kirkpatrick AW,Cresswell AB, Malbrain M, Bodnar Z, Mejia-Mantilla JH, Reis R,Parr M, Schulze R, Compano S, Cheatham M: The effect ofdifferent reference transducer positions on intra-abdominalpressure measurement: a multicenter analysis. Intensive CareMed 2008, 34:1299-303.

12. McBeth PB, Zygun DA, Widder S, Cheatham M, Zengerink I, Glowa J,Kirkpatrick AW: Effect of patient positioning on intra-abdom-inal pressure monitoring. Am J Surg 2007, 193:644-7; discussion647.

13. Malbrain ML: Is it wise not to think about intraabdominalhypertension in the ICU? Curr Opin Crit Care 2004, 10:132-45.

14. De laet I, Malbrain ML: ICU management of the patient withintra-abdominal hypertension: what to do, when and towhom? Acta Clin Belg Suppl 2007, 62:190-9.

15. De laet I, Citerio G, Malbrain ML: The influence of intraabdom-inal hypertension on the central nervous system: currentinsights and clinical recommendations, is it all in the head?Acta Clin Belg Suppl 2007, 62:89-97.

16. Citerio G, Vascotto E, Villa F, Celotti S, Pesenti A: Inducedabdominal compartment syndrome increases intracranialpressure in neurotrauma patients: a prospective study. CritCare Med 2001, 29:1466-71.

17. Bloomfield GL, Ridings PC, Blocher CR, Marmarou A, Sugerman HJ:Effects of increased intra-abdominal pressure upon intracra-nial and cerebral perfusion pressure before and after volumeexpansion. J Trauma 1996, 40:936-41; discussion 941-3.

18. Bloomfield GL, Ridings PC, Blocher CR, Marmarou A, Sugerman HJ: Aproposed relationship between increased intra-abdominal,intrathoracic, and intracranial pressure. Crit Care Med 1997,25:496-503.

19. Miele VJ, Bendok B, Bloomfield SM, Ondra SL, Bailes JE: Ventricu-loperitoneal shunt dysfunction in adults secondary to condi-tions causing a transient increase in intra-abdominalpressure: report of three cases. Neurosurgery 2004, 55:434.

20. Cheatham ML, Malbrain ML: Cardiovascular implications ofabdominal compartment syndrome. Acta Clin Belg Suppl 2007,62:98-112.

21. Renner J, Gruenewald M, Quaden R, Hanss R, Meybohm P, Scholz J,Bein B: Influence of increased intra-abdominal pressure onfluid responsiveness predicted by pulse pressure variationand stroke volume variation in a porcine model. Crit Care Med2009, 37:650-8.

22. Gruenewald M, Renner J, Meybohm P, Hocker J, Scholz J, Bein B:Reliability of continuous cardiac output measurement duringintra-abdominal hypertension relies on repeated calibrations:an experimental animal study. Crit Care 2008, 12:R132.

23. Ridings PC, Bloomfield GL, Blocher CR, Sugerman HJ: Cardiopul-monary effects of raised intra-abdominal pressure before andafter intravascular volume expansion. J Trauma 1995, 39:1071-5.

24. Pelosi P, Quintel M, Malbrain ML: Effect of intra-abdominalpressure on respiratory mechanics. Acta Clin Belg Suppl 2007,62:78-88.

25. Quintel M, Pelosi P, Caironi P, Meinhardt JP, Luecke T, Herrmann P,Taccone P, Rylander C, Valenza F, Carlesso E, Gattinoni L: Anincrease of abdominal pressure increases pulmonary edemain oleic acid-induced lung injury. Am J Respir Crit Care Med 2004,169:534-41.

26. Talmor D, Sarge T, O’Donnell CR, Ritz R, Malhotra A, Lisbon A,Loring SH: Esophageal and transpulmonary pressures in acuterespiratory failure. Crit Care Med 2006, 34:1389-94.

27. Wendon J, Biancofiore G, Auzinger G: Intra-abdominal hyperten-sion and the liver. In Abdominal Compartment Syndrome. Edited byIvatury R, Cheatham M, Malbrain M, Sugrue M: Georgetown: LandesBioscience; 2006:138-43.

28. Biancofiore G, Bindi ML, Boldrini A, Consani G, Bisà M, Esposito M,Urbani L, Catalano G, Filipponi F, Mosca F: Intraabdominalpressure in liver transplant recipients: incidence and clinicalsignificance. Transplant Proc 2004, 36:547-9.

29. Michelet P, Roch A, Gainnier M, Sainty JM, Auffray JP, Papazian L:Influence of support on intra-abdominal pressure, hepatickinetics of indocyanine green and extravascular lung waterduring prone positioning in patients with ARDS: a rando-mized crossover study. Crit Care 2005, 9:R251-7.

30. Sugrue M, Hallal A, D’Amours S: Intra-abdominal pressurehypertension and the kidney. In Abdominal Compartment Syndrome.Edited by Ivatury R, Cheatham M, Malbrain M, Sugrue M. Georgetown:Landes Bioscience; 2006:119-28.

31. Sugrue M, Jones F, Deane SA, Bishop G, Bauman A, Hillman K: Intra-abdominal hypertension is an independent cause of post-operative renal impairment. Arch Surg 1999, 134:1082-5.

32. Dalfino L, Tullo L, Donadio I, Malcangi V, Brienza N: Intra-abdominal hypertension and acute renal failure in criticallyill patients. Intensive Care Med 2008, 34:707-13.

33. Kirkpatrick AW, Colistro R, Laupland KB, Fox DL, Konkin DE,Kock V, Mayo JR, Nicolaou S: Renal arterial resistive indexresponse to intraabdominal hypertension in a porcine model.Crit Care Med 2007, 35:207-13.

34. De Waele JJ, Hoste EA, Malbrain ML: Decompressive laparotomyfor abdominal compartment syndrome–a critical analysis. CritCare 2006, 10:R51.

Page 7 of 7(page number not for citation purposes)

F1000 Medicine Reports 2009, 1:86 http://F1000.com/Reports/Medicine/content/1/86